Morphological features of structure of aorta, coronal arteries and myocardium at chronic kidneys disease
DOI:
https://doi.org/10.15587/2313-8416.2015.57234Keywords:
Morphology, aorta, coronary arteries, chronic pulmonary disease, VEGF, bcl-2Abstract
The most important functions of endothelium are: hemostasis regulation, inflammation modulation, vascular tone correction, vascular permeability regulation. Chronic pulmonary disease (CPD) breaks this balance and predisposes vessels to vasoconstriction, leukocyte adhesion, platelet activation, mitogenesis, inflammation. The aim of the work was to study morphological changes of the cardiovascular walls and aorta in patients with CPD and to assess the possibilities of its endothelium to reparation.
Materials and methods. There was studied an autopsy material of 18 died persons 45-55 years old. All died persons had the signs of chronic pulmonary disease (CPD).
For detection of the immune cellular reaction features in zone of inflammation process there were used the primary homogenous antibodies (HGAB) of DAKO (Denmark), Rady-to-Use.
The studies were carried out on microscope Primo Star (Carl Zeiss) using AxioCam (ERc 5s).
Results and discussion: The changes of endothelium of coronary vessels of heart and aorta were demonstrated with the different degree of disorganization. These pathologic processes were familiar to the immune inflammation. The weak expression of the growth factor of VEGF and bcl-2 vessels endothelium can be the indirect sign of the low ability of the vascular wool structure and endothelium lining to reconstruction because an activation of apoptosis takes place at its deficiency.
Conclusions. The changes of coronary arteries and aorta construction at CPD are characterized with unidirectional nature with the different intensity of pathologic process in all layers of the vascular wall and vascular transformation that is typical for immune inflammation. The detected disorders of vascular morphology and immunoinflammatory reaction activity can be the one of the main causes of cardiovascular complications development
References
Yamamoto, S., Kon, V. (2009). Mechanisms for increased cardiovascular disease in chronic kidney dysfunction. Current Opinion in Nephrology and Hypertension, 18 (3), 181–188. doi: 10.1097/mnh.0b013e328327b360
Parikh, N. I., Hwang, S.-J., Larson, M. G., Levy, D., Fox, C. S. (2008). Chronic Kidney Disease as a Predictor of Cardiovascular Disease (from the Framingham Heart Study). The American Journal of Cardiology, 102 (1), 47–53. doi: 10.1016/j.amjcard.2008.02.095
Telo, P., Lostaglio, S., Dejana, E. (1997). Structure of intercellular junctions in the endothelium. Therapie, 52 (5), 395–398.
Schiffrin, E. L., Lipman, M. L., Mann, J. F. E. (2007). Chronic Kidney Disease: Effects on the Cardiovascular System. Circulation, 116 (1), 85–97. doi: 10.1161/circulationaha.106.678342
Yamamoto, S., Kon, V. (2009). Mechanisms for increased cardiovascular disease in chronic kidney dysfunction. Current Opinion in Nephrology and Hypertension, 18 (3), 181–188. doi: 10.1097/mnh.0b013e328327b360
Verma, S. (2002). Fundamentals of Endothelial Function for the Clinical Cardiologist. Circulation, 105 (5), 546–549. doi: 10.1161/hc0502.104540
Tangri, N., Komenda, P.V., Rigatto, C. (2015). Chronic kidney disease and heart disease: after 179 years, do we yet understand the link? Kidney International, 88, 11–13. doi: 10.1038/ki.2015.112
Buske-Kirschbaum, A., Kern, S., Ebrecht, M., Hellhammer, D. H. (2007). Altered distribution of leukocyte subsets and cytokine production in response to acute psychosocial stress in patients with psoriasis vulgaris. Brain, Behavior, and Immunity, 21 (1), 92–99. doi: 10.1016/j.bbi.2006.03.006
Menges, P., Kessler, W., Kloecker, C., Feuerherd, M., Gaubert, S., Diedrich, S. et. al. (2012). Surgical Trauma and Postoperative Immune Dysfunction. European Surgical Research, 48 (4), 180–186. doi: 10.1159/000338196
Manjarrez-Orduño, N., Moreno-García, M. E., Fink, K., Santos-Argumedo, L. (2007). CD38 cross-linking enhances TLR-induced B cell proliferation but decreases IgM plasma cell differentiation. European Journal of Immunology, 37 (2), 358–367. doi: 10.1002/eji.200636453
Zhao, J., Zhao, S., Zhou, G., Liang, L., Guo, X., Mao, P. et. al. (2011). Altered biliary epithelial cell and monocyte responses to lipopolysaccharide as a TLR ligand in patients with primary biliary cirrhosis. Scandinavian Journal of Gastroenterology, 46 (4), 485–494. doi: 10.3109/00365521.2010.539624
Bittencourt, M. S., Hulten, Е. А., Ghoshhajra, В., Abbara, S, Murthy, V. L., Divakaran, S., Nasir, K., Gowdak, L. H., Riella, L. V., Chiumiento, M., Hoffmann, U., Di Carli, M. F., Blankstein, R. (2015). Incremental prognostic value of kidney function decline over coronary artery disease for cardiovascular event prediction after coronary computed. Kidney International, 88, 152–159. doi: 10.1038/ki.2014.426
Downloads
Published
Issue
Section
License
Copyright (c) 2015 Ирина Ивановна Яковцова, Иван Иванович Топчий, Светлана Владимировна Данилюк, Александр Николаевич Кириенко, Денис Александрович Кириенко
This work is licensed under a Creative Commons Attribution 4.0 International License.
Our journal abides by the Creative Commons CC BY copyright rights and permissions for open access journals.
Authors, who are published in this journal, agree to the following conditions:
1. The authors reserve the right to authorship of the work and pass the first publication right of this work to the journal under the terms of a Creative Commons CC BY, which allows others to freely distribute the published research with the obligatory reference to the authors of the original work and the first publication of the work in this journal.
2. The authors have the right to conclude separate supplement agreements that relate to non-exclusive work distribution in the form in which it has been published by the journal (for example, to upload the work to the online storage of the journal or publish it as part of a monograph), provided that the reference to the first publication of the work in this journal is included.
